ArticleInflammation2020
Luteolin and Apigenin Attenuate LPS-Induced Astrocyte Activation and Cytokine Production by Targeting MAPK, STAT3, and NF-κB Signaling Pathways.
Article in Inflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 64 citations in OpenAlex.
- Therapeutic potential of apigenin in neurodegenerative diseases and brain health.Molecular biology reports · 2026Review
- Apigenin as a Potential Modulator of Neuroinflammation in Multiple Sclerosis: A Review.Biology · 2026Review
- From Claims to Evidence: Re-Evaluating the Molecular Pharmacology ofInternational journal of molecular sciences · 2026Review
- Apigenin Mitigates PFOA-Induced Activation of the NLRP3-Pyroptosis Axis and Associated Neurological Damage.Environment & health (Washington, D.C.) · 2026Article
- Neuroprotective effects of luteolin against aluminum-induced brain injury via chelation and antioxidant pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Neuroprotective Effects of Sorghum Polyphenol in Alzheimer's Disease: In Vitro and In Silico Analyses.Nutrients · 2026Article
- Comparative Phytochemical Profiling and Wound Healing Potential ofFood science & nutrition · 2026Article
- In Vitro Antioxidant Activity and In Vivo Neuroprotective Effect ofAntioxidants (Basel, Switzerland) · 2025Article
- Anti-Oxidant, Anti-Inflammatory and Antiviral Properties of Luteolin Against SARS-CoV-2: Based on Network Pharmacology.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Anti-Inflammatory Actions of Plant-Derived Compounds and Prevention of Chronic Diseases: From Molecular Mechanisms to Applications.International journal of molecular sciences · 2025Review
- Antipruritic Effect of 2,3-Dehydrosilybin in Glial Cells and Chloroquine-Treated Mice.Journal of microbiology and biotechnology · 2025Article
- Anti-Inflammatory Mechanisms ofJournal of microbiology and biotechnology · 2025Article
- Article
- Therapeutic Expedition of Luteolin against Brain-related Disorders: An Updated Review.Combinatorial chemistry & high throughput screening · 2025Review
- Anti-CLL1 liposome loaded with miR-497-5p and venetoclax as a novel therapeutic strategy in acute myeloid leukemia.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Review of the potential value of serum interleukin levels as prognostic biomarkers of liver failure.World journal of clinical cases · 2024Review
- Nebulized Lipopolysaccharide Causes Delayed Cortical Neuroinflammation in a Murine Model of Acute Lung Injury.International journal of molecular sciences · 2024Article
- Natural Flavonoid Apigenin, an Effective Agent Against Nervous System Cancers.Molecular neurobiology · 2024Review
- Luteolin for neurodegenerative diseases: a review.Pharmacological reports : PR · 2024Review
- Polyphenols Targeting MAP Kinase Signaling Pathway in Neurological Diseases: Understanding Molecular Mechanisms and Therapeutic Targets.Molecular neurobiology · 2024Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Astrocytes release biologically active substances that cause inflammation in neurodegenerative diseases. The present study investigated the effects of two flavonoids (apigenin and luteolin) on the production of IL-31 and IL-33 in lipopolysaccharide (LPS)-activated astrocytes. Cell viability was investigated using EZ-Cytox assay, mRNA expressions of IL-31 and IL-33 were analyzed by RT-PCR, protein expressions were analyzed by western blot, and cytokine secretion was analyzed by ELISA. Apigenin and luteolin prevented astrocyte activation and inhibited mRNA and protein expression and secretion of IL-31 and IL-33 in the LPS-treated astrocytes. Apigenin's suppression of ERK, NF-κB, and STAT3 activations was responsible for the inhibition of IL-31 and IL-33, while luteolin's suppression of JNK, p38, ERK, NF-κB, and STAT3 activations was responsible for the inhibition of IL-31 in the astrocytes. Also, luteolin's suppression of ERK, NF-κB, and STAT3 activations inhibited IL-33 production in the activated astrocytes. In addition, apigenin and luteolin also prevented the translocation of activated STAT3 and NF-κB to the nucleus of the activated astrocytes and subsequently affected their DNA binding activities. The results suggest that apigenin and luteolin may have potentials as neuroprotective agents for the treatment of diseases involving astrocyte activation and detrimental production of IL-31 and IL-33.
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Registered trials
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